QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

This Article Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (24) Citing Articles via Google Scholar Google Scholar Articles by Treistman, S. N. Articles by Wilson, A. Search for Related Content PubMed PubMed Citation Articles by Treistman, S. N. Articles by Wilson, A.

 Previous Article  |  Next Article 

Journal of Neuroscience, Vol 7, 3207-3214, Copyright © 1987 by Society for Neuroscience

ARTICLE

Effects of ethanol on early potassium currents in Aplysia: cell specificity and influence of channel state

SN Treistman and A Wilson
Worcester Foundation for Experimental Biology, Shrewsbury, Massachusetts 01545.

The effects of ethanol (EtOH) on the early potassium current, IA, were examined in 3 identified neurons of Aplysia using voltage-clamp techniques. The primary effect of EtOH on this current was a pronounced increase in the time constant of decay. However, this effect was cell specific, being evident in cells MCC and R15 but not in cell B1. Other parameters of IA were not greatly affected in any of the cells, in comparison with the effects on decay time constant. Baseline parameters of IA were measured in each of the cells to determine whether subpopulations of IA channel might exist, and be differentially sensitive to EtOH. While differences did appear among cells, they were not consistent with an explanation of EtOH's actions based upon distribution of channel subtypes. The effect of EtOH on IA decay was dependent upon the voltage-clamp protocol used. When inactivation of IA developed at -20 mV, the slower development of inactivation noted above occurred. When inactivation without channel opening was produced by means of a prepulse to -40 mV, EtOH speeded up the development of inactivation. A number of possible explanations for these findings are discussed. Most of the effects of EtOH occurred within 1 min of application of the drug, suggesting relatively rapid access to the site of action. Effects continued to develop over succeeding minutes. This slower-developing effect may reflect either a delayed access to channels due to slower diffusion into or lateral movement within the lipid phase of the membrane, or it may indicate that channels are accessible to the EtOH molecule only when in certain states.

This article has been cited by other articles:

				A. M Dopico, H. Widmer, G. Wang, J. R Lemos, and S. N Treistman Rat supraoptic magnocellular neurones show distinct large conductance, Ca2+-activated K+ channel subtypes in cell bodies versus nerve endings J. Physiol., August 15, 1999; 519(1): 101 - 114. [Abstract] [Full Text] [PDF]

				S. I. Alekseev, A. S. Alekseev, and M. C. Ziskin Effects of Alcohols on A-Type K+ Currents in Lymnaea Neurons J. Pharmacol. Exp. Ther., April 1, 1997; 281(1): 84 - 92. [Abstract] [Full Text]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help